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We report a case of a 57-year-old immunocompetent male, admitted to our Department due to the loss of visual acuity to the right eye, occurred during the two weeks before the hospitalization, and hyperglycaemia. Our patient suffered from metabolic syndrome, characterized by visceral obesity, impaired glucose tolerance, arterial hypertension, complicated by proteinuria, and moderate grade hypertensive retinopathy. Surprisingly, and despite its many comorbidities, the final diagnosis was neuroretinitis by Bartonella henselae, without any other symptoms/signs of cat-scratch disease. The patient denied any kind of contact with cats. He was cured by specific antibiotic therapy, restoring status ‘quo ante’.

Food allergy is a common and increasing problem worldwide. The newly-found knowledge might provide novel experimental strategies, especially for laboratory diagnosis. Approximately 20% of the population alters their diet for a perceived adverse reaction to food, but the application of double-blind placebo-controlled oral food challenge, the “gold standard” for diagnosis of food allergy, shows that questionnaire-based studies overestimate the prevalence of food allergies. The clinical disorders determined by adverse reactions to food can be classified on the basis of immunologic or nonimmunologic mechanisms and the organ system or systems affected. Diagnosis of food allergy is based on clinical history, skin prick tests, and laboratory tests to detect serum-food specific IgE, elimination diets and challenges. The primary therapy for food allergy is to avoid the responsible food. Antihistamines might partially relieve oral allergy syndrome and IgE-mediated skin symptoms, but they do not block systemic reactions. Systemic corticosteroids are generally effective in treating chronic IgE-mediated disorders. Epinephrine is the mainstay of treatment for anaphylaxis. Experimental therapies for IgE-mediated food allergy have been evaluated, such as humanized IgG anti-IgE antibodies and allergen specific immunotherapy.

The role of helminths in asthma and/or rhinitis and in allergic sensitization is still unclear. We assessed the relationship between Ascaris-specific IgE, respiratory symptoms and allergic sensitization in Bangladesh immigrants. 246 individuals were examined from 1996 to 2001. Serum total IgE, Ascaris IgE, specific IgE to inhalant allergens, skin prick tests (SPT) and parasitological evaluation of the stool were performed. Total serum IgE were significantly higher in Ascaris-IgE positive (> 0.35 kU/L) individuals (806.5 [409.0–1436.0] kU/L vs. 207.0 [127.0–332.5] kU/L; P < 0.0001) and in subjects with respiratory symptoms (413.0 [239.0–1096.0] kU/L vs. 259.5 [147.0–387.0] kU/L), ( P < 0.0001), but not in SPT positive subjects (413.0 [179.0–894.0] kU/L vs. 404.6 [305.0–1201.0] kU/L ( P= 0.5). Ascaris-specific IgE were detected in 48 subjects with respiratory symptoms (40.0%) and in 46 subjects without respiratory symptoms (36.5%) ( P = 0.5). The SPT positivity was similar between Ascaris-IgE seropositive (38.2%) and Ascaris-IgE seronegative (38.1%) subjects ( P = 0.9). Total IgE and length of stay in Italy correlated with SPT positivity (OR 5.6 [CI 95% 1.5–19.8], P = 0.007, and OR 1.5 [CI 95% 1.3–1.7], P < 0.0001), and with respiratory symptoms (OR 13.7 [CI 95% 3.0–62.4], P = 0.0007, and OR 2.4 [CI 95% 1.9–3.0], P < 0.0001). Ascaris-IgE were negatively associated with SPT positivity (OR 0.3 [CI 95% 0.1–0.8], P = 0.02) and with respiratory symptoms (OR 0.1 [CI 95% 0.04–0.7], P = 0.01). Our findings favour the role of environmental factors in the development of respiratory symptoms in immigrants, irrespective of Ascaris-IgE.

Subjects with rhinitis but without asthma may have coexisting bronchial hyperresponsiveness, although the reasons for this are uncertain. To evaluate the factors that determine BHR in rhinitis we examined 410 patients with symptomatic rhinitis with forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) ≥ 80% of the predicted value. In all subjects a skin prick test (SPT) was performed, a determination of total serum IgE and an eosinophils count in the blood. Of the 410 subjects we found that 161 (39.3%) exhibited a methacholine PD20 of 800 mg or less (Group A), whereas 249 (60.7%) had a methacholine PD20 more of 800 mg (Group B). Despite the matched mean values for FEV1 and FVC, compared with Group B, Group A had a lower predicted forced expiratory flow between 25% and 75% (FEF25%-75%) (86.7 ± 12.0 vs. 93.7±7.3, P < 0.0001). A great portion of the subjects of the Group A in respect to subjects of the Group B were exposed to passive smoke (37.8% vs. 22.0%, P = 0.0008), reported having mothers with asthma (34.1% vs. 6.0%, P < 0.0001), presented a positive skin prick test (93.7% vs. 67.0%, P < 0.0001), had higher levels of total serum IgE (geometric mean of Log10 2.46 ± 0.27 kU/L vs. 2.06 ± 0.38 kU/L, P < 0.0001) and higher blood eosinophil counts (geometric mean of Log10 2.67 ± 0.07 × 10−3 mL vs. 2.57 ± 0.09 × 10−3 mL, P < 0.0001), and reported increased nasal obstruction (2.0 (95%CI 1.8 to 2.2) vs. 0.6 (95%CI 0.5 to 0.7), P < 0.0001). Logistic regression demonstrates that nasal obstruction (OR 2.19,95%CI 1.72 to 2.80) and the presence of positive SPT (OR 6.15,95%CI 2.42 to 15.61) were the most available predictors to discriminate between subjects with BHR and subjects without BHR. In addition, BHR was positively related to blood eosinophil counts (OR= 2.80, 95%CI 1.54 to 5.07), FEF25%-75% values (OR= 2.72, 95%CI 1.23 to 5.99) and familiarity (mother) for asthma (OR = 2.45, 95%CI 1.10 to 5.46). Whereas passive smoke and total serum IgE were not positively related to BHR. Increased nasal obstruction and the presence of positive SPT were the most available predictors to discriminate between subjects with and without BHR. Finally, BHR was positively related to blood eosinophil counts, FEF25%-75% values and to familiarity (mother) for asthma.